Patent law rests on a simple covenant: inventors reveal their secrets, and society grants them temporary monopolies in return. But some companies want the monopoly without the showing. They want the treasure. They don’t want to draw the map.
In 2014, Amgen had developed evolocumab—a protein comprising 1,328 amino acids arranged with such precision that changing even one could eliminate its function entirely. This antibody binds to PCSK9, a protein that destroys the liver’s cholesterol-clearing receptors, and block its activity completely.
Amgen filed patents describing evolocumab in exhaustive detail. Twenty-five additional antibodies followed—all synthesized, all tested, all real. Then they claimed ownership of millions more they had never made.
That claim would soon be tested. Three thousand miles away, Regeneron had developed an entirely different antibody called alirocumab. Different sequence, different structure, different discovery method. It blocked the same protein.
The FDA blessed both drugs within twenty-eight days that summer of 2015—a bureaucratic miracle that should have marked the triumph of competitive innovation. Instead, Amgen was making the opening moves to an enormous legal assault——one that had begun the prior autumn. Nearly a decade later, nine Supreme Court justices would determine whether building a mousetrap grants you dominion over every possible way to catch a mouse.
Two Paths to the Same Summit
To understand what Amgen was claiming, we need to venture briefly into the cellular processes where this story unfolds.
Picture the liver cell as a recycling facility where LDL receptors serve as loading docks, constantly pulling cholesterol particles from the bloodstream for processing and disposal. PCSK9 functions as a quality control mechanism in this system. Its job—refined over millions of years of evolution—is to bind these receptors and mark them for destruction. When food was scarce and humans faced frequent starvation, this made evolutionary sense. PCSK9 helped conserve every molecule of cholesterol during lean times.
But evolution optimizes for survival to reproductive age, not for the convenience of modern medicine. In a world of drive-throughs and desk jobs, PCSK9’s cholesterol-conserving function has become a liability, contributing to the plaques that trigger heart attacks and strokes.
The protein’s importance emerged through one of biology’s elegant accidents. In the early 2000s, researchers had found genetic lottery winners—a French-Canadian family with naturally inactive PCSK9 who maintained cholesterol levels below 50 mg/dL and remarkably clear arteries well into old age.
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